Gene/Protein Disease Symptom Drug Enzyme Compound
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 21,692 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mental symptoms increased in frequency among 100 patients with parkinsonism treated with levodopa. Dementia was found in about one-third of patients throughout the 6-year treatment period. Thirteen patients became demented during the study, and dementia worsened severely in seven others. Agitated confusion became increasingly frequent and was observed in 60 percent of patients taking levodopa for 6 years. Withdrawal from levodopa decreased agitation, but not dementia. Ten patients received L-tryptophan along with levodopa, but no change in mentation was observed. In view of previous studies of mentation in Parkinson's disease and reports of widespread neuronal changes in the brain of autopsied patients with parkinsonism, our results suggest that the high incidence of dementia in patients with Parkinson's disease who take levodopa reflects prolongation of the course of the illness rather than a direct effect of the medication.
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PMID:Mental symptoms in Parkinson's disease during chronic treatment with levodopa. 94 87

The responses of thirteen patients with bulimia nervosa and sixteen controls matched for age and weight are described following the ingestion of a carbohydrate and a calorie-free placebo mixture in simulated binges. Psychological, hormonal and biochemical parameters were measured before and at 15 minute intervals for two hours after the simulated binge. At baseline, the bulimics were clearly more symptomatic than the controls. The control population showed a specific satiating effect of carbohydrate upon hunger ratings. Bulimic patients responded differently showing a blunting of the normal sensation of hunger and an enhanced rating for nausea. Prolactin, growth hormone (GH) and cortisol failed to show a carbohydrate-mediated stimulation in either population. The bulimic patients showed a different pattern of GH release, but this was independent of the challenge condition. Large neutral amino acid (LNAA) levels fell following carbohydrate ingestion, but produced an increase of up to 20% in the tryptophan: LNAA ratio in both bulimic patients and the control group. Thus, while this increase in tryptophan availability failed to provoke hormone release, the time course of the carbohydrate specific effect on the sensations of hunger and nausea is compatible with a mechanism based on increased tryptophan availability. The confusion of satiety with nausea may provide a useful focus for the future treatment of patients with bulimia nervosa.
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PMID:Psychological, hormonal and biochemical changes following carbohydrate bingeing: a placebo controlled study in bulimia nervosa and matched controls. 204 88

The serotonin syndrome has increasingly been recognised in patients who have received combined serotonergic drugs. This syndrome is characterised by a constellation of symptoms (confusion, fever, shivering, diaphoresis, ataxia, hyperelflexia, myoclonus or diarrhoea) in the setting of the recent addition of a serotonergic agent. The most common drug combinations causing the serotonin syndrome are monoamine oxidase inhibitors (MAOIs) and serotonin selective reuptake inhibitors (SSRIs), MAOIs and tricyclic antidepressants, MAOIs and tryptophan, and MAOIs and pethidine (meperidine). This syndrome is caused by excess serotonin (5-hydroxytryptamine; 5-HT) availability in the CNS at the 5-HT1A-receptor. There may also be some interaction with dopamine and 5-HT2-receptors. This syndrome probably has a low incidence, even among patients taking these drug combinations, and there is likely to be some other as yet unidentified inciting factor causing some patients to develop a full serotonin syndrome. Because fatalities and severe complications have accompanied the serotonin syndrome, the previously described drug combinations should be used cautiously or not at all. The serotonin syndrome is usually mild and, if managed with drug withdrawal and supportive therapy, generally improves within hours. Patients who develop hyperthermia should be treated aggressively with external cooling and paralysis. Methysergide and cyproheptadine appear to be useful adjuncts in treating the serotonin syndrome.
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PMID:The serotonin syndrome. Implicated drugs, pathophysiology and management. 757 68

We describe a patient treated with trazodone, isocarboxazid, and methylphenidate hydrochloride who developed confusion, agitation, poor concentration, rigidity, myoclonus, involuntary movements, orthostatic hypotension, and hyperreflexia. CK was normal, and the syndrome resolved spontaneously over 12 hours. The serotonin syndrome occurs following the use of serotomimetic agents (serotonin reuptake inhibitors, tricyclic and tetracyclic antidepressants, tryptophan, 3,4-methylenedioxy-methamphetamine, dextromethorphan, meperidine, S-adenosylmethionine) alone or in combination with monoamine oxidase inhibitors. It is characterized by various combinations of myoclonus, rigidity, hyperreflexia, shivering, confusion, agitation, restlessness, coma, autonomic instability, low-grade fever, nausea, diarrhea, diaphoresis, flushing, and rarely, rhabdomyolysis and death.
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PMID:Serotonin syndrome. 785 15

In animals the occurrence of a behavioural syndrome consisting of hyperactivity, stereotyped movements and increase of temperature has been induced by MAOIs, 5-HT precursors (L-tryptophan) and 5-HT reuptake inhibitors. Most of these manifestations were specifically blocked by a pretreatment with an inhibitor of serotonin synthesis. In humans, the association of myoclonus, diarrhea, confusion, hypomania, agitation, hyperreflexia, shivering, incoordination, fever and diaphoresis, when patients are treated with serotoninergic agents, could constitute a "serotonin syndrome". Such cases of serotonin syndrome were reported after treatments with L-tryptophan, MAOIs, serotonin reuptake inhibitors and tricyclics alone or in association. The authors prospectively evaluated all the "serotonin-related" symptoms in 38 depressed inpatients fulfilling DSM III-R criteria of major depression. 16 (42%) out of 38 patients presented at least one symptom of serotonin syndrome. In 14 cases tremor and myoclonus occurred simultaneously and 10 patients presented at the same time tremor, myoclonus, diaphoresis and shivering. Except for two patients, symptoms were transient, lasted less than one week and disappeared with the pursuit of the treatment. Most often, serotonin syndrome thus corresponds to a reaction induced by a combination of serotoninergic agents at high dosages. In very rare cases, a toxic and potentially fatal interaction can occur between MAOIs, tricyclics and selective serotonin reuptake inhibitors at therapeutic dosages. Serotonin syndrome also provides an heuristic model of the putative mode of action of antidepressants. Serotonin-related symptoms are the physical and objective expression of the antidepressant-induced increase in serotonin. The specificity of serotonin-related syndrome also needs to be discussed since most of the symptoms, such as tremor and diaphoresis, are not in all cases related to an increase in serotonin.
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PMID:[The serotonin syndrome: review of the literature and description of an original study]. 852 62

Acute eosinophilia-myalgia syndrome (EMS) due to contaminated L-tryptophan (LT) exposure is an inflammatory microangiopathy of the dermis, fascia, and muscle. Select individuals evolve from acute EMS to have persistence of myalgia, fatigue, cramps, and skin changes for years. Many develop memory dysfunction and confusion. The objective of this study is to delineate the pathology in individuals with chronic EMS. Seventeen patients with ongoing symptoms representing chronic EMS are studied by skin, fascia, and muscle biopsies four to five years after exposure to contaminated LT and initial onset of EMS. All have microvascular disease. Most have lymphocytic inflammatory infiltrates. Several have dermal sclerosis. The findings indicate that persistent microvascular disease is present in chronic EMS. The pathologic changes are similar to those of acute EMS but with notable differences. Tissue eosinophil infiltration is rare in the chronic state as compared to acute EMS. The persistence of endothelial pathology indicates continuing microvascular dysfunction.
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PMID:Persistent microvasculopathy in chronic eosinophilia-myalgia syndrome. 890 89

The serotonin syndrome is frequently characterized by minor neurologic manifestations that regress rapidly (such as confusion, tremor, ...). Many medications including tricyclic antidepressants, serotonin reuptake inhibitors, tryptophan and the association of monoamine oxidase inhibitors together with a serotoninergic agent have been implicated in this syndrome. In certain cases, and for poorly understood reasons, clinical manifestations can include circulatory collapse, malignant hyperthermia, convulsions and rhabdomyolysis. These forms are often fatal. Treatment, other than the withdrawal of the offending drug, is symptomatic. Dialysis may be of value in withdrawing the drug from the circulatory system. We report a patient with the serotonin syndrome of favorable outcome due to an overdose of moclobemide and clomipramine.
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PMID:Serotonin syndrome due to an overdose of moclobemide and clomipramine. A potentially life-threatening association. 903 53

23% of all septic patients develop septic encephalopathy which is associated with an increased mortality rate. Symptoms such as agitation, confusion and disorientation ranging from stupor to coma often develop in early sepsis. Severe hypotension is significantly associated with the development of septic encephalopathy. Several other factors which may play a role are also discussed: effects of inflammatory mediators on the brain, inadequate cerebral perfusion pressure, blood-brain barrier derangements, disturbances of the cerebral microcirculation, cerebral ischemia e.g. due to hypocapnia,metabolic changes, altered amino acid levels, transmitter imbalances, liver insufficiency, multiple organ failure and infections of the CNS, respectively. Compared to patients with an isolated infection,patients in septic shock have increased levels of aromatic amino acids such as phenylalanine and tryptophan in the plasma and brain as well as decreased levels of branched chain amino acids. Patients who died had higher levels of aromatic amino acids than the survivors. The correlation between aromatic amino acids and the APACHE II score was significant. The tryptophan metabolite quinolinic acid which can be synthesized in activated macrophages could act as an excitatory transmitter on the N-methyl-D-aspartate (NMDA) -receptor. Observations from experimental models indicate that activated NMDA receptors activate the neuronal isoform of the NO-synthase and other calcium dependent enzymes. This releases free radicals which may damage the DNA and activate the nuclear enzyme Poly-ADP-ribose-synthetase (PARS), resulting in energy depletion and cell death. Sepsis is the main cause of metabolic encephalopathies in critically ill patients. The differential diagnoses include hepatic, renal,hypoxic-ischemic or cardiovascular encephalopathies as well as encephalopathies,metabolic disorders and organ dysfunctions of other origin. Therapeutic interventions are numerous,however, so far only investigated in few controlled studies. The primary therapeutic goal is to maintain an adequate perfusion pressure and to prevent hypoxia and hypocapnia. Although the infusion of branched chain amino acids is controversial, experimental investigations demonstrated improvements improvements in an animal model with septic encephalopathy. Further investigations with respect to glutamate receptor antagonists, new radical scavengers, NO- and PARS-inhibitors may show whether these substances are suitable for the prophylaxis or early therapy of septic encephalopathy.
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PMID:[Septic encephalopathy. Diagnosis und therapy]. 1275 14

Oxidation of proteins with performic acid is extensively used to cleave disulfide bonds. Due to its efficiency and many other advantages it deserves more attention especially in proteomics as a method for sample treatment. However, some unwanted degradations can occur during performic oxidation. In this work the degradation products during performic oxidation of two peptides and bovine serum albumin as model substrates were explored by coupling high-performance liquid chromatography (HPLC) to matrix-assisted laser desorption/ionization tandem mass spectrometry (MALDI-TOF/TOFMS). In addition to well-known modifications such as oxidation of tryptophan and oxidation and chlorination of tyrosine, novel degradation products including nonspecific cleavage after asparagine or tryptophan, formylation of lysine, and beta-elimination of cysteine, were observed. Although almost all of these modification/degradation products except oxidation products of tryptophan were formed at sub-stoichiometric levels, they can cause confusion as a result of the sensitivity of mass spectrometry in analysis of the oxidized samples, especially in proteomics research. The results presented here will facilitate the interpretation of analytical data for performate-oxidized samples, and help to select appropriate methods for each unique sample.
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PMID:Identification of degradation products formed during performic oxidation of peptides and proteins by high-performance liquid chromatography with matrix-assisted laser desorption/ionization and tandem mass spectrometry. 1579 70

This study assessed the effects of acute tryptophan depletion (ATD), which transiently lowers CNS 5-HT, on electrocortical responses to facial expression processing in individuals with a family history of depression (FH+). Electroencephalograph (EEG)-derived event-related potentials (ERPs) were acquired from 18 FH+ individuals during a facial expression recognition task (neutral and sad, joy and surprise at 50% and 100% intensities). Both early positive (P1 and P2) and the face-specific N170 ERP components were differentially altered by emotional intensity and valence. Increased depression, confusion and total mood disturbance scores, and decreased calmness, were observed with ATD (versus placebo). ATD was also associated with enhanced P1 and P2 amplitudes for sad versus joyful expressions. The N170 was not modulated by treatment, but was affected by emotive valence. Therefore, ATD enhanced ERP-indexed early processing of sad facial expressions, and altered the processing of positive ones, in FH+ individuals.
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PMID:Electrocortical effects of acute tryptophan depletion on emotive facial processing in depression-prone individuals. 2039 15


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